Comparison of generalized autocalibrating partially parallel acquisitions and modified sensitivity encoding for diffusion tensor imaging.

BACKGROUND AND PURPOSE: Diffusion tensor magnetic resonance imaging (DTI) of the brain is usually acquired with single-shot echo-planar imaging, which is associated with localized signal loss, geometric distortions, and blurring. Parallel imaging can lessen these artifacts by shortening the length of the echo-train acquisition. The self-calibrating parallel acquisition techniques, image domain-based modified sensitivity encoding (mSENSE) and k-space-based generalized autocalibrating partially parallel acquisitions (GRAPPA), were evaluated with DTI of the brain in 5 healthy subjects. METHODS: GRAPPA and mSENSE with higher acceleration factors (R) up to 4 were compared with conventional DTI (with and without phase partial Fourier, another method of reducing the echo-train length) on a 1.5T Sonata scanner (Siemens, Erlangen, Germany). The resulting images and diffusion maps were evaluated qualitatively and quantitatively. Qualitative analysis was performed by 3 reviewers blinded to the technique using image sharpness and the level of artifacts as characteristics for scoring each set of images. Quantitative comparisons encompassed measuring signal-to-noise ratio, Trace/3 apparent diffusion coefficient (ADC), and fractional anisotropy (FA) in 6 white-matter (WM) and gray-matter (GM) regions. RESULTS: Reviewers scored the GRAPPA and mSENSE R = 2 images better than images acquired with conventional techniques. FA contrast was improved at the GM/WM junction in peripheral brain areas. Trace/3 ADC and FA measurements were consistent for all methods. However, R = 3,4 images suffered from reconstruction-related artifacts. CONCLUSIONS: GRAPPA and mSENSE (R = 2) minimized the susceptibility and off-resonance effects associated with conventional DTI methods, yielding high-quality images and reproducible quantitative diffusion measurements.

Magnetic resonance imaging predicts neuropathology from soman-mediated seizures in the rodent.

Intoxication by the organophosphate compound soman causes prolonged seizures that lead to neuropathology in the brain. This MRI-based study describes the temporal and spatial evolution of brain pathology that follows soman-induced convulsions. We observed significant decreases in apparent diffusion coefficients (ADC; 23% below control) of the hippocampus and thalamus by 12 h after soman treatment. The ADC then returned to near normal values in all regions at 24 h but declined again during the next 7 days. These data suggest that the initial cellular degradation may be resolved but is ultimately followed by regional cellular remodeling. T2 relaxation values declined significantly at 12 h (37% decrease) returning to near normal values by 24 h. These data lend detail to the model suggesting that injured tissues experience an edematous influx that is resolved by 24 h. The imaging data was fully supported by histopathological comparisons where moderate cell loss and swelling within the hippocampus and piriform cortex was observed. This is the first report providing excellenttemporal and spatial resolution of emerging soman-mediated, seizure-induced neuropathology using MRI with histological correlation.

Benzolamide, acetazolamide, and signal transduction in avian intrapulmonary chemoreceptors.

Intrapulmonary chemoreceptors (IPC) are CO(2)-sensitive sensory neurons that innervate the lungs of birds, help control the rate and depth of breathing, and require carbonic anhydrase (CA) for normal function. We tested whether the CA enzyme is located intracellularly or extracellularly in IPC by comparing the effect of a CA inhibitor that is membrane permeable (iv acetazolamide) with one that is relatively membrane impermeable (iv benzolamide). Single cell extracellular recordings were made from vagal filaments in 16 anesthetized, unidirectionally ventilated mallards (Anas platyrhynchos). Without CA inhibition, action potential discharge rate was inversely proportional to inspired PCO(2) (-9.0 +/- 0.8 s(-1). lnTorr(-1); means +/- SE, n = 16) and exhibited phasic responses to rapid PCO(2) changes. Benzolamide (25 mg/kg iv) raised the discharge rate but did not alter tonic IPC PCO(2) response (-9.8 +/- 1.6 s(-1). lnTorr(-1), n = 8), and it modestly attenuated phasic responses. Acetazolamide (10 mg/kg iv) raised IPC discharge, significantly reduced tonic IPC PCO(2) response to -3.5 +/- 3.6 s(-1). lnTorr(-1) (n = 6), and severely attenuated phasic responses. Results were consistent with an intracellular site for CA that is less accessible to benzolamide. A model of IPC CO(2) transduction is proposed.