British Journal of Radiology (2004) 77, 528-531
© 2004 British Institute of Radiology
doi: 10.1259/bjr/51430802
Delayed post-contrast fluid-attenuated inversion recovery image for depicting meningeal carcinomatosis
T Hirota, MD
K Ishihara, MD, PhD
K Akazawa, MD
T Kubota, MD
K Yamada, MD, PhD
and
T Nishimura, MD, PhD
Department of Radiology, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo, Kyoto, 602-8566, Japan
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Abstract
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We present a case of intracranial meningeal carcinomatosis that was visualized more clearly on a delayed contrast-enhanced fluid-attenuated inversion recovery (FLAIR) MRI than on other regular post-contrast MRI.
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Introduction
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The most specific diagnostic method for intracranial meningeal carcinomatosis is cytological examination of cerebrospinal fluid (CSF). This method, however, often produces false-negative results. MRI, especially contrast enhanced T1 weighted image, are regarded as a reliable technique for confirming the diagnosis and for assessing the extent of the lesions and response to therapy [19]. Recently, contrast-enhanced fluid-attenuated inversion recovery (FLAIR) MRI have been described as a useful technique for diagnosing meningeal diseases [7, 1012]. In this report, we describe a case in which intracranial meningeal carcinomatosis was visualized more clearly on delayed contrast enhanced FLAIR images than on conventional post-contrast MRI, including enhanced T1 weighted images, enhanced FLAIR, and delayed contrast-enhanced T1 weighted images.
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Case report
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A 60-year-old woman presented with rapidly progressing ataxia, disorientation and epileptic seizures over a 1 month period. Her past medical history prior to admittance at this hospital included adenocarcinoma of the lung, for which she had undergone partial resection and chemotherapy. Her physical examination and laboratory data were unremarkable. A chest radiograph revealed a large mass in the right lung, indicative of recurrent lung cancer.
A CT of the brain demonstrated dilatation of the lateral ventricles suggesting hydrocephalus. Brain MRIs were performed using a 0.5 T superconducting whole-body MR unit (Flexart; Toshiba, Tokyo, Japan). Unenhanced T1 and T2 weighted images were obtained, followed by enhanced T1 weighted and FLAIR images using intravenous administration of gadopentetate dimeglumine (Magnevist; Schering, Berlin, Germany). The unenhanced FLAIR image that is part of our routine scan protocol was omitted because of the urgency of the examination. The unenhanced T1 (Figure 1a
) and T2 weighted (Figure 1b
) images confirmed the known hydrocephalus. T1 weighted and FLAIR images were obtained soon after the intravenous administration of 0.1 mmol kg1 of gadopentetate dimeglumine (these initial examinations are hereafter referred to as "early-enhanced" studies). The early-enhanced T1 weighted image (Figure 1c
) did not demonstrate any area of abnormal enhancement. The early-enhanced FLAIR image (Figure 1e
) revealed an abnormal hyperintensity in the anterior interhemispheric fissure and left inferior temporal sulci, although these findings were inconclusive as to whether they represented enhanced or unenhanced lesions, since the pre-contrast FLAIR images had been omitted. To clarify these observations, the T1 weighted and FLAIR images were repeated 2 h after administration of the contrast (these subsequent examinations are hereafter referred to as "delayed-enhanced" studies). The delayed-enhanced T1 weighted image (Figure 1d
) did not demonstrate any abnormal enhancement. The delayed-enhanced FLAIR image (Figure 1f
) demonstrated a more conspicuous abnormal hyperintensity along the sulci than in the early-enhanced FLAIR image, not only in the anterior interhemispheric fissure and left inferior temporal sulci, but also in other regions of the CSF spaces, such as the bilateral sylvian fissure and basal cistern. We concluded that the image findings represented the leakage of the administered contrast materials into the CSF through the destroyed bloodbrain barrier (BBB), which strongly indicates intracranial meningeal carcinomatosis. A lumbar puncture was performed immediately after the second MR examination. The CSF cytology revealed adenocarcinoma cells, and the patient was diagnosed as having intracranial meningeal carcinomatosis originating from her known lung cancer.


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Figure 1. (a) Axial unenhanced T1 weighted (590/15) [repetition time ms/echo time ms] and (b) T2 weighted (3500/120) images do not show any remarkable findings, except for hydrocephalus. (c) Axial early- and (d) delayed-enhanced T1 weighted (590/15) images obtained soon and 2 h after the intravenous administration of contrast materials, respectively, fail to demonstrate the presence of abnormal CSF or meningeal enhancement. (e) Axial early-enhanced FLAIR (8000/120/1900) [repetition time ms/ echo time ms/ inversion time ms] image obtained soon after the intravenous administration of contrast materials shows an abnormal hyperintensity in the anterior interhemispheric fissure (arrow) and the left inferior temporal sulci (open arrow). (f) Axial delayed-enhanced FLAIR (8000/120/1900) image obtained 2 h after the intravenous administration of contrast materials shows an apparent abnormal hyperintensity in the bilateral sylvian fissures (open arrows). The anterior interhemispheric fissure (arrow) and the left inferior temporal sulci (solid arrow) also show an abnormal hyperintensity on the delayed enhanced FLAIR image, when compared with the early-enhanced FLAIR image.
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Discussion
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Intracranial meningeal carcinomatosis is a devastating complication of malignancy and is found in approximately 5% of cancer patients at autopsy [13], and the incidence appears to be increasing [14, 15]. The disease is most commonly seen in patients with breast and lung cancer, and melanoma. Most commonly presenting with focal neurological signs, the prognosis for these patients is poor, with a median survival of only 4 to 6 weeks if left untreated and 2 to 3 months with treatment [13, 16]. Early diagnosis of meningeal carcinomatosis is important, as there is evidence that suggests early treatment with intrathecal methotrexate and radiotherapy may prolong survival [14, 1719].
Intracranial meningeal carcinomatosis is diagnosed clinically from the patients neurological symptoms and radiological findings on CT or MRI. The diagnosis may be confirmed by examination of CSF from a lumbar puncture. However, positive CSF cytology is found on initial lumbar puncture in only 50% of patients with meningeal carcinomatosis [16, 20]. MRIs are regarded as a reliable technique for confirming the diagnosis and for assessing the extent of the lesions and response to therapy. Unfortunately, contrast-enhanced MRI is insensitive with reported sensitivities of up to 71% [1, 2].
The MRI findings of meningeal carcinomatosis are hydrocephalus, dural and leptomeningeal enhancement, and subependymal enhancement [1, 2, 8, 9, 2124]. Traditionally, a contrast enhanced T1 weighted sequence has been the preferred sequence in diagnosis and follow-up [19]. Recent studies [11, 25] have indicated that post-contrast FLAIR images are sometimes more useful for detecting intraparenchymal lesions than post-contrast T1 weighted images. Post-contrast FLAIR images have been shown to be more effective in demonstrating meningeal lesions than post-contrast T1 weighted images, possibly because FLAIR is more sensitive at demonstrating lower concentrations of contrast than T1 weighted images, as indicated in a phantom study by Mathews et al [11]. The usefulness of contrast-enhanced FLAIR images as a diagnostic tool has been increasingly described [7, 1012, 25].
In our case, meningeal abnormalities were only suggested on the early-enhanced FLAIR images, from the initial series of sequences. The abnormal hyperintensity seen was suggestive of meningeal disease, although it was uncertain at this point whether or not the findings were real. The second delayed examination was performed to confirm the abnormality. Pui et al [8] suggested that delayed T1 weighted images might improve the detection of CSF enhancement in meningeal carcinomatosis. Furthermore, as discussed earlier [11], FLAIR images may be more sensitive than T1 weighted images at demonstrating lower concentrations of contrast, as seen in our case.
Following the observation in the present case, we are currently assessing the use of this technique in a prospective study. To our knowledge, this is the first report describing the usefulness of delayed-enhanced FLAIR images for the diagnosis of meningeal disease.
In summary, we have shown that abnormal areas of hyperintensity observed on early-enhanced FLAIR images can be confirmed using delayed-enhanced FLAIR images. For the diagnosis of intracranial meningeal diseases, equivocal findings depicted on early-enhanced FLAIR images can be confirmed using delayed-enhanced FLAIR images.
Received for publication July 2, 2002.
Revision received July 17, 2003.
Accepted for publication October 2, 2003.
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