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A comprehensive model of the BOLD response is presented, in which differential equations for cerebral O2 and hemoglobin (Hgb) transport are solved numerically. Several features of cerebral O2 transport can be investigated, and the consistency of current conceptions of BOLD responses tested. This study applies the model to the effects of arterial hematocrit, PaCO2 and PaO2, in responses elicited by functional activation (fBOLD) and physiological pertubation (pBOLD). The model uses 4 major compartments: arterial, capillary and venous as well as an extravascular compartment. Within the intravascular compartment the distribution of O2 between Hgb-bound and physically dissolved phases is updated for every time step, t, as a function of local pH, PCO2 and DPG. Total content of deoxy-Hgb is calculated as the sum of arterial, capillary and venous concentrations weighted by their respective volume fractions. The corresponding R2*-contribution is calculated as proposed by Ogawa et al. (1993). Relationships between PaO2, PaCO2 and CBF, as well as between CBF and CBV were taken from previous studies. The model predicted BOLD effects of the expected magnitude (1–3% at 1.5 T), and confirmed an inverse relation between fBOLD and baseline CBF. A slight decrease in fBOLD response was seen with high baseline hematocrit and constant CBF, but an increase was seen when concomitant flow decreases were included (in agreement with empirical results). During hypercapnia the predicted pBOLD response was high when CBF changes alone were included (figure 1: green curve), but attenuated by the accompanying CBV change (blue curve). The response was elevated when all effects were included (red curve), mainly due to the effect of arterial hyperoxia (hyperventilation), less to pH changes. Several physiological effects thus were predicted in accordance with established results. The model suggests that known effects of hematocrit may be due to accompanying flow changes. During hypercapnia, arterial hyperoxia is an important factor which should be taken into account when used in calibration experiments for CMRO2 determination. Numerical simulation seems helpful in interpreting BOLD effects caused by complex physiological responses.

We sought to assess whether magnetic resonance imaging (MRI) at 3.0 T detects more brain lesions in acute optic neuritis (ON) than MRI at 1.5 T.Twenty-eight patients with acute ON were scanned at both field-strengths using fast-fluid-attenuated inversion recovery (FLAIR), proton density and T2-weighted turbo spin echo, and T1-weighted spin echo after contrast. In addition, magnetization-prepared rapid acquisition gradient echo (MPRAGE) was obtained after contrast at 3.0 T. Lesion number and volumes were assessed by an observer blind to patient identity and field strength.Scans at 3.0 T showed a significantly increase in number of lesions detected on FLAIR images (P = 0.002) relative to scanning at 1.5 T. MPRAGE proved to be suitable for detecting enhancing lesions in ON.The MRI protocol at 3.0 T was more sensitive to hyperintense brain lesions in ON than the standard MRI protocol at 1.5 T.

Analysis of fMRI time series is often performed by extracting one or more parameters for the individual voxels. Methods based, e.g., on various statistical tests are then used to yield parameters corresponding to probability of activation or activation strength. However, these methods do not indicate whether sets of voxels are activated in a similar way or in different ways. Typically, delays between two activated signals are not identified. In this article, we use clustering methods to detect similarities in activation between voxels. We employ a novel metric that measures the similarity between the activation stimulus and the fMRI signal. We present two different clustering algorithms and use them to identify regions of similar activations in an fMRI experiment involving a visual stimulus.

The purpose of this study was to determine whether the capillary transfer constant (Ki) of gadolinium-DTPA was sensitive to perfusion changes and whether ischemic regions in the myocardium could be identified using the modified Kety formula. Ki was measured at rest and during dipyridamole-induced vasodilation in 10 healthy volunteers and in 10 patients with ischemic heart disease. Ki increased by a factor of 2.5+/-1.2 (mean +/- SD) from 55+/-16 ml 100 g(-1)min(-1) at rest to 136+/-46 ml 100 g(-1)min(-1) (P0.01) during vasodilation in the healthy subjects. In the patients, there were no changes in Ki during vasodilation in ischemic regions (50+/-18 versus 49+/-30 ml 100 g(-1)min(-1) (P0.4)). Ki increased in nonischemic regions by a factor of 2.0+/-0.8 from 44+/-17 to 81+/-32 ml 100 g(-1)min(-1) during vasodilation (P0.02). It is concluded that the capillary transfer constant is sensitive to perfusion changes and that regional ischemia can be detected with MRI. This noninvasive and quantitative method may prove useful in the evaluation of patients with ischemic heart disease.

The blood oxygenation level-dependent (BOLD) effect in functional magnetic resonance imaging depends on at least partial uncoupling between cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) changes. By measuring CBF and BOLD simultaneously, the relative change in CMRO2 can be estimated during neural activity using a reference condition obtained with known CMRO2 change. In this work, nine subjects were studied at a magnetic field of 1.5 T; each subject underwent inhalation of a 5% carbon dioxide gas mixture as a reference and two visual stimulation studies. Relative CBF and BOLD signal changes were measured simultaneously using the flow-sensitive alternating inversion recovery (FAIR) technique. During hypercapnia established by an end-tidal CO2 increase of 1.46 kPa, CBF in the visual cortex increased by 47.3 +/- 17.3% (mean +/- SD; n = 9), and deltaR2* was -0.478 +/- 0.147 sec(-1), which corresponds to BOLD signal change of 2.4 +/- 0.7% with a gradient echo time of 50 msec. During black/white visual stimulation reversing at 8 Hz, regional CBF increase in the visual cortex was 43.6 +/- 9.4% (n = 18), and deltaR2* was -0.114 +/- 0.086 sec(-1), corresponding to a BOLD signal change of 0.6 +/- 0.4%. Assuming that CMRO2 does not change during hypercapnia and that hemodynamic responses during hypercapnia and neural stimulation are similar, relative CMRO2 change was determined using BOLD biophysical models. The average CMRO2 change in the visual cortex ranged from 15.6 +/- 8.1% (n = 18) with significant cerebral blood volume (CBV) contribution to 29.6 +/- 18.8% without significant CBV contribution. A weak positive correlation between CBF and CMRO2 changes was observed, suggesting the CMRO2 increase is proportional to the CBF increase.

To introduce dynamic magnetic resonance imaging (MRI) as an indicator of inflammatory activity in the metacarpophalangeal (MCP) joints of patients with rheumatoid arthritis (RA) or early unclassified polyarthritis, and to compare the results with a healthy control group.We examined 42 RA and 23 early unclassified polyarthritis patients, and 12 healthy controls in a cross-sectional study. Dynamic MRI (repeated FLASH-MR images after injection of a contrast agent) was performed through the 2nd to the 5th MCP joint. Two methods for identification of the enhancing synovial membrane were compared: 1) outlining of enhancing synovial membrane on subtraction images and 2) automated recognition by principal component analysis (PCA). The early enhancement (EE) rate was calculated on the basis of the first method.Method 1) and 2) were closely associated (P0.00001). From the healthy control group, an upper limit (mean+2SD) of normal enhancement was established for the 2nd to 5th MCP joints, which served to identify abnormal EE rates in the corresponding joints of patients. The patients had higher EE rates in the 2nd to 5th MCP joints than had the healthy controls (P0.01). There were no significant differences between the two patient groups (P0.09).PCA seems to be a promising method for automated identification of enhancing tissue. EE rates of the finger joints may be useful in the assessment of the inflammatory activity in the joints of patients with RA and early unclassified polyarthritis and may reflect other aspects of disease activity than clinical evaluation.

A noninvasive method using an inversion recovery turbo-FLASH for dynamic measurement of the arterial input function represented by the bolus passage of Gd-DTPA in the descending aorta is presented, and the results are compared with the input function obtained by arterial blood samples. A good accordance between the two input functions was found, indicating that it is possible to measure the input function to the myocardium using MRI. A variation between the two concentration curves of 5% at upslope, 2.7% at peak point, and < 7% at downslope was found. The study also indicates that a short inversion time < 250 ms has to be used to ensure correct measurement of peak concentration.

Alterations in cerebral resting-state functional connectivity (RSFC) have been reported outside of migraine attacks. To date, no studies studied possible changes in RSFC during migraine attacks.