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In reference to 3 Tesla Delayed Contrast Magnetic Resonance Imaging Evaluation of Meniere's Disease

We read with great interest the article by Carfrae et al.1 in the section published ahead of print December 18, 2007. To us, a radiologist and otorhinolaryngologist who are specialized in temporal bone magnetic resonance imaging (MRI) in research and clinical practice for about 20 years, several issues in the article raised serious concerns. The authors tried to visualize endolymphatic hydrops using 3-Tesla MRI with triple-dose intravenous administration of gadolinium (Gd) contrast agent. In the first part of their study, they tried to determine the timing of maximum contrast enhancement in four normal subjects. They stated that all four normal subjects demonstrated clear perilymph enhancement between 2 and 4 hours after contrast injection. However, the results of signal intensity measurements at 4 hours (shown in Fig. 1) revealed a relatively small enhancement compared with the precontrast state (13–20%). The signal intensity values of MRI are not absolute; thus, if they needed to discuss such a small enhancement, they should have stated that the measured value was signal-to-noise ratio or relative signal intensity (the signal of interest divided by nonenhancing brain parenchyma signal, or preferably, that of an external phantom). In the postcontrast images shown in Figures 2–5, labyrinthine fluid showed a far brighter signal than the brain. Though they did not show any precontrast images, we assume that the labyrinthine signal was higher than that of brain parenchyma even on precontrast images. If labyrinthine fluid showed a higher signal than brain parenchyma on precontrast images, then the images were not properly T1-weighted to detect the T1shortening effect caused by Gd-diethylenetriaminopentaacetic acid (DTPA). Furthermore, the images they refer to as “T1 delayed images” (shown in Figs. 2–5) do not seem to be sufficiently T1-weighted. These images show no contrast between gray and white matter of the brain (no intensity difference), though gray-white contrast is a characteristic of truly T1-weighted images. Cerebrospinal fluid in the internal auditory canal and the sulcus of the cerebellar hemisphere also showed higher signals than brain. These images should be referred to as proton density-weighted images or T2/T1-weighted images, but such images are not as sensitive as proper T1weighted images to the positive contrast enhancement of Gd-DTPA. Low signal in the prepontine cistern, cerebellopontine angle cistern, and fourth ventricle is thought to be due to the flow of cerebrospinal fluid. We think that the authors should have shown precontrast images to make their results more convincing to their readers. The authors stated in the introduction section that “the time for Gd contrast diffusion into the perilymph is not known in humans.” However, there was a previous study using 3-Tesla MRI showing that maximal labyrinthine enhancement occurs 4 hours after intravenous injection of Gd-DTPA.2 This study had been published before Carfrae et al.1 presented their results at the meeting in Chicago. In this previous study, appropriately T1-weighted images failed to detect perilymph enhancement. Instead, 3D-fluid attenuated inversion recovery (FLAIR) images were used to detect very low concentrations of Gd-DTPA in the labyrinth. 3D-FLAIR is more sensitive to low concentrations of Gd-DTPA than T1-weighted images.2 In a more recent study using intratympanic injection of Gd-DTPA, 3D-FLAIR was mainly used because even optimal T1-weighted images cannot detect enhancement of perilymph.3 We do not believe that intravenously injected Gd-DTPA would be visibly detected on T1-weighted images, even with triple-dose Gd-DTPA, proper scan timing, and 3-Tesla MRI. Visual recognition of perilymphatic enhancement is crucial for the visual recognition of endolymphatic hydrops. In the second part of their study, the authors scanned patients with Meniere’s disease. However, the abnormal image findings they showed were not convincing. They stated that 5 of 7 diseased ears showed a loss of radiological definition of cochlear architecture, such as a loss of definition of scala tympani. In cases of endolymphatic hydrops, scala media extend and scala vestibuli should be compressed. However, scala tympani would not be influenced to such an extent, even if there was some shift of the basilar membrane. Thus, we cannot determine whether the figures showing patients’ ears in the present study demonstrate pathological changes due to endolymphatic hydrops or not. In conclusion, the visualization of endolymphatic space in humans has not been accomplished with intravenous Gd-DTPA injection yet, as the authors stated. The visualization of endolymphatic space is the most important key to the direct diagnosis of Meniere’s disease. So far, the visualization of endolymphatic space has only been done through intratympanic injection of Gd-DTPA with 3D-FLAIR imaging at 3 Tesla.3