Diffuse Dural Enhancement on MRI: Not a Sign of Leptomeningeal Cancer
ABSTRACT & COMMENTARY
Source: River Y, et al. Clinical significance of diffuse dural enhancement detected by magnetic resonance imaging. J Neurosurg 1996;85:777-783.
Two patterns of meningeal enhancement can be recognized when contrast is used with MRI. Leptomeningeal enhancement appears either as a thin line or small nodules that closely follow the gyral convolutions. Dural enhancement is visible underneath the inner table of the skull and can be either focal or diffuse.
Focal dural enhancement is characteristic of meningiomas. Diffuse dural enhancement (DDE), although uncommon, has multiple causes: chronic meningitis, subdural hemorrhage, craniotomy, intracranial hypotension, primary and metastatic tumors, and, perhaps, as claimed by some, even leptomeningeal metastases.
In order to determine the clinical significance of DDE and identify patterns related to inflammatory or neoplastic causes, River et al evaluated 20 patients with DDE encompassing at least 75% of the dural surface.
In 13 patients, DDE was associated with malignancy. Ten had skull metastases, two had primary CNS tumors: medulloblastoma and malignant melanoma. One patient had breast cancer with both leptomeningeal and skull metastases. In five patients, DDE was caused by intracranial hypotension due to CSF leak or ventricular shunting; one patient had sagittal sinus thrombosis, another had pachymeningitis on dural biopsy.
Clinical findings in these 20 patients were compared to 11 consecutive patients with leptomeningeal cancer documented by malignant cells in the CSF. None of these 11 had DDE, but two had leptomeningeal enhancement and two focal dural enhancement.
Clinical findings were otherwise identical in the two groups: headache, cranial nerve palsies, and elevated CSF protein. Two patients with leptomeningeal cancer had hypoglycorrhachia.
COMMENTARY
In this series, most of the patients with DDE (13/20, 65%) had an underlying malignancy associated with skull metastases. Only 7 of 20 (35%) had non-neoplastic etiologies. Although the pathophysiological mechanisms inducing DDE are not fully understood, it appears to be a diffuse inflammatory reaction rather than a neoplastic growth. Even in patients with skull metastases DDE may reflect periosteal reaction rather than tumor invasion. The cranial nerve involvement associated with DDE probably reflects a compressive neuropathy induced by thickening of the dural sleeves of the CN nerves.
In contrast, leptomeningeal cancer causes enhancement by disrupting the blood-brain barrier at sites of direct tumor invasion of the subarachnoid space. Hence, the findings in this series that none of 11 patients with leptomeningeal metastasis presented with DDE.
Nevertheless, the common clinical manifestations of DDE and leptomeningeal cancer were indistinguishable, and one patient in the series had both DDE due to skull metastases and leptomeningeal enhancement due to leptomeningeal cancer. Therefore, although the authors have shown that DDE and leptomeningeal cancer are different entities both pathophysiologically and radiographically, the fact is that DDE due to malignancy can coexist with leptomeningeal metastases. This means that an LP with examination of CSF cytology remains a necessary part of the evaluation of a symptomatic patient with a pattern of DDE on contrast-enhanced MRI.
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