Cerebrospinal Fluid T1 Research Articles

Optimization of the fluid-attenuated inversion recovery (FLAIR) imaging for use in autopsy imaging of the brain region using synthetic MRI.

The failure of cerebrospinal fluid (CSF) signal suppression in postmortem fluid-attenuated inversion recovery (FLAIR) of the brain is a problem. The present study was to clarify the relationship between the temperature of deceased persons and CSF T1, and to optimize the postmortem brain FLAIR imaging method using synthetic MRI. Forehead temperature was measured in 15 deceased persons. Next, synthetic MRI of the brain was performed, the CSF T1 was measured, and the optimal TI was calculated. Two types of FLAIR images were obtained with the clinical and optimal TI. The relationship between forehead temperature and the CSF T1 and optimal TI was evaluated. The optimized FLAIR images were physically and visually evaluated. The CSF T1 and optimal TI were strongly correlated with forehead temperature. Comparing the average SNR and CNR ratios and visual evaluation scores of the two FLAIR images, those captured with the optimal TI showed statistically lower SNR, higher CNR, and higher visual evaluation scores (p< 0.01). Synthetic MRI enables the quantification of the CSF T1 resulting from postmortem temperature decreases and calculation of the optimal TI, which could aid in improving the failure of CSF signal suppression and in optimizing postmortem brain FLAIR imaging.

Brain Morphometry and Longitudinal Relaxation Time of Spontaneously Hypertensive Rats (SHRs) in Early and Intermediate Stages of Hypertension Investigated by 3D VFA-SPGR MRI

Cerebral small vessel disease(s) (SVD) results from pathological changes of the small blood vessels in the brain and is common in older people. The diagnostic features by which SVD manifests in brain includes white matter hyperintensities, lacunes, dilated perivascular spaces, microbleeds, and atrophy. In the present study, we use in vivo magnetic resonance imaging (MRI) to characterize brain morphometry and longitudinal relaxation time (T1) of spontaneously hypertensive rats (SHRs) to study the contribution of chronic hypertension to SVD relevant pathology. Male SHR and Wistar-Kyoto (WKY) rats underwent 3D variable flip angle spoiled gradient echo brain MRI at 9.4 T at early (seven weeks old) and established (19 weeks old) stages of hypertension. The derived proton density weighted and T1 images were utilized for morphometry and to characterize T1 properties in gray matter (GM), white matter (WM) and cerebrospinal fluid (CSF). Custom tissue probability maps were constructed for accurate computerized whole brain tissue segmentations and voxel-wise analyses. Characteristic morphological differences between the two strains included enlarged ventricles, smaller corpus callosum (CC) volumes and general ‘thinning’ of CC in SHR compared to WKY rats at both age groups. While we did not observe parenchymal T1 differences, the T1 of CSF was elevated in SHR compared to controls. Collectively these findings indicate that SHRs develop WM atrophy which is a clinically robust MRI biomarker associated with WM degeneration.

Myelin water mapping by spatially regularized longitudinal relaxographic imaging at high magnetic fields

Magnetic resonance T1 -weighted images are routinely used for human brain segmentation, brain parcellation, and clinical diagnosis of demyelinating diseases. Myelin is thought to influence the longitudinal relaxation commonly described by a mono-exponential recovery, although reports of bi-exponential longitudinal relaxation have been published. The purpose of this work was to investigate if a myelin water T1 contribution could be separated in geometrically sampled Look-Locker trains of low flip angle gradient echoes. T1 relaxograms from normal human brain were computed by a spatially regularized inverse Laplace transform after estimating the apparent inversion efficiency. With sufficiently long inversion-time sampling (ca. 5 × T1 of cerebrospinal fluid), the T1 relaxogram revealed a short-T1 peak (106-225 ms). The apparent fraction of this water component increased in human brain white matter from 8.3% at 3 T, to 11.3% at 4 T and 15.0% at 7 T. The T2 * of the short-T1 peak at 3 T was shorter, 27.9 ± 13.0 ms, than that of the long-T1 peak, 51.3 ± 5.6 ms. The short-T1 fraction is interpreted as the water resident in myelin. Its detection is facilitated by longer T1 of axoplasmic water at higher magnetic field.

Measurement of cerebrospinal fluid oxygen partial pressure in humans using MRI

Fluid-attenuated inversion recovery (FLAIR) images obtained during the administration of supplemental oxygen demonstrate a hyperintense signal within the cerebrospinal fluid (CSF) that is likely caused by T1 changes induced by paramagnetic molecular oxygen. Previous studies demonstrated a linear relationship between the longitudinal relaxation rate (R1 = 1/T1) and oxygen content, which permits quantification of the CSF oxygen partial pressure (P(csf)O2). In the current study, CSF T1 was measured at 1.5 T in the lateral ventricles, third ventricle, cortical sulci, and basilar cisterns of eight normal subjects breathing room air or 100% oxygen. Phantom studies performed with artificial CSF enabled absolute P(csf)O2 quantitation. Regional P(csf)O2 differences on room air were observed, from 65 +/- 27 mmHg in the basilar cisterns to 130 +/- 49 mmHg in the third ventricle. During 100% oxygen, P(csf)O2 increases of 155 +/- 45 and 124 +/- 34 mmHg were measured in the basilar cisterns and cortical sulci, respectively, with no change observed in the lateral or third ventricles. P(csf)O2 measurements in humans breathing room air or 100% oxygen using a T1 method are comparable to results from invasive human and animal studies. Similar approaches could be applied to noninvasively monitor oxygenation in many acellular, low-protein body fluids.

The Effect of Intravenous Gadolinium on the Magnetic Resonance Appearance of Cerebrospinal Fluid

The authors determined whether a sufficient amount of intravenously administered gadolinium enters the cerebrospinal fluid (CSF) to visibly shorten the T1 relaxation time. Transfer of intravenously administered contrast media into the CSF has been previously documented for iodinated contrast materials; however, the change in computed tomography density is not sufficient to have a clinically useful myelographic effect. Visible shortening of the T1 of CSF on gadolinium-enhanced magnetic resonance imaging of the spine may have clinical use. Twelve dogs were given gadolinium, and CSF was sampled at intervals over a 6-hour period. The T1 values of the CSF samples were quantitated and plotted against time. The average decrease in T1 was 23% at 60 minutes, which is nearly the peak effect. The increased signal intensity was visible at clinical window settings at 60 minutes. It is possible that this may be clinically useful for certain types of examinations. Importantly, this should be recognized as a normal appearance, and not necessarily a sign of pathology.

Cyclophosphamide plasma and cerebrospinal fluid kinetics with and without dimethyl sulfoxide.

Ten patients with brain tumors and indwelling ventricular reservoirs were pretreated with 5% to 10% dimethyl sulfoxide (DMSO) (intravenous, oral, or both) and were then treated with 1.0 to 1.25 gm/m2 cyclophosphamide (CYC). All patients were also on anticonvulsants and dexamethasone. CYC and alkylating activity (alk act) in plasma and concomitant ventricular cerebrospinal fluid (CSF) were measured by gas chromatography and p-nitrobenzyl pyridine assay. CYC entered the CSF without difficulty and was lost from CSF more slowly than from plasma. Alk act did not enter CSF as well as did CYC. DMSO did not alter any measured aspect of CYC or alk act disposition. Specifically, it did not alter the CYC plasma half-life (t1/2), CSF t1/2, peak CSF: peak plasma CYC concentration ratio, or the urinary excretion of CYC. DMSO did not alter the plasma t1/2 or urinary excretion of alk act or the peak CSF:peak plasma concentration ratio of alk act. Our data show reduced plasma t1/2 of CYC and increased plasma and urinary alk act. This may reflect tht effect of long-term therapy with anticonvulsants or steroids.