Image quality and cancer visibility of T2-weighted magnetic resonance imaging of the prostate at 7 Tesla.

OBJECTIVES: To assess the image quality of T2-weighted (T2w) magnetic resonance imaging of the prostate and the visibility of prostate cancer at 7 Tesla (T). MATERIALS & METHODS: Seventeen prostate cancer patients underwent T2w imaging at 7T with only an external transmit/receive array coil. Three radiologists independently scored images for image quality, visibility of anatomical structures, and presence of artefacts. Krippendorff's alpha and weighted kappa statistics were used to assess inter-observer agreement. Visibility of prostate cancer lesions was assessed by directly linking the T2w images to the confirmed location of prostate cancer on histopathology. RESULTS: T2w imaging at 7T was achievable with 'satisfactory' (3/5) to 'good' (4/5) quality. Visibility of anatomical structures was predominantly scored as 'satisfactory' (3/5) and 'good' (4/5). If artefacts were present, they were mostly motion artefacts and, to a lesser extent, aliasing artefacts and noise. Krippendorff's analysis revealed an α = 0.44 between three readers for the overall image quality scores. Clinically significant cancer lesions in both peripheral zone and transition zone were visible at 7T. CONCLUSION: T2w imaging with satisfactory to good quality can be routinely acquired, and cancer lesions were visible in patients with prostate cancer at 7T using only an external transmit/receive body array coil. KEY POINTS: • Satisfactory to good T2-weighted image quality of the prostate is achievable at 7T. • Periprostatic lipids appear hypo-intense compared to healthy peripheral zone tissue at 7T. • Prostate cancer is visible on T2-weighted MRI at 7T.

Quantitative short echo time 1H MRSI of the peripheral edematous region of human brain tumors in the differentiation between glioblastoma, metastasis, and meningioma.

PURPOSE: To assess metabolite levels in peritumoral edematous (PO) and surrounding apparently normal (SAN) brain regions of glioblastoma, metastasis, and meningioma in humans with (1)H-MRSI to find biomarkers that can discriminate between tumors and characterize infiltrative tumor growth. MATERIALS AND METHODS: Magnetic resonance (MR) spectra (semi-LASER MRSI, 30 msec echo time, 3T) were selected from regions of interest (ROIs) under MRI guidance, and after quality control of MR spectra. Statistical testing between patient groups was performed for mean metabolite ratios of an entire ROI and for the highest value within that ROI. RESULTS: The highest ratios of the level of choline compounds and the sum of myo-inositol and glycine over N-acetylaspartate and creatine compounds were significantly increased in PO regions of glioblastoma versus that of metastasis and meningioma. In the SAN region of glioblastoma some of these ratios were increased. Differences were less prominent for metabolite levels averaged over entire ROIs. CONCLUSION: Specific metabolite ratios in PO and SAN regions can be used to discriminate glioblastoma from metastasis and meningioma. An analysis of these ratios averaged over entire ROIs and those with most abnormal values indicates that infiltrative tumor growth in glioblastoma is inhomogeneous and extends into the SAN region.

The role of pressurized fluid in subchondral bone cyst growth.

Pressurized fluid has been proposed to play an important role in subchondral bone cyst development. However, the exact mechanism remains speculative. We used an established computational mechanoregulated bone adaptation model to investigate two hypotheses: 1) pressurized fluid causes cyst growth through altered bone tissue loading conditions, 2) pressurized fluid causes cyst growth through osteocyte death. In a 2D finite element model of bone microarchitecture, a marrow cavity was filled with fluid to resemble a cyst. Subsequently, the fluid was pressurized, or osteocyte death was simulated, or both. Rather than increasing the load, which was the prevailing hypothesis, pressurized fluid decreased the load on the surrounding bone, thereby leading to net bone resorption and growth of the cavity. In this scenario an irregularly shaped cavity developed which became rounded and obtained a rim of sclerotic bone after removal of the pressurized fluid. This indicates that cyst development may occur in a step-wise manner. In the simulations of osteocyte death, cavity growth also occurred, and the cavity immediately obtained a rounded shape and a sclerotic rim. Combining both mechanisms increased the growth rate of the cavity. In conclusion, both stress-shielding by pressurized fluid, and osteocyte death may cause cyst growth. In vivo observations of pressurized cyst fluid, dead osteocytes, and different appearances of cysts similar to our simulation results support the idea that both mechanisms can simultaneously play a role in the development and growth of subchondral bone cysts.