The integrity of frontal-striatal circuits is an area of great interest in substance dependence literature, particularly as the field begins to develop neural circuit-specific brain stimulation treatments for these individuals. Prior research indicates that frontal-striatal connectivity is disrupted in chronic cocaine users in a baseline (resting) state. It is unclear, however, if this is also true when these circuits are mobilized by an external source. In this study, we measured the functional and structural integrity of frontal-striatal circuitry involved in limbic arousal and executive control in 36 individuals-18 cocaine-dependent individuals with a history of failed quit attempts and 18 age-matched controls. This was achieved by applying a transcranial magnetic stimulation to the medial prefrontal cortex (Brodmann area 10) and the dorsolateral prefrontal cortex (lateral Brodmann 9) while participants rested in the MRI scanner (TMS/BOLD imaging). Relative to the controls, cocaine users had a lower ventral striatal BOLD response to MPFC stimulation. The dorsal striatal BOLD response to DLPFC stimulation however was not significantly different between the groups. Among controls, DLPFC stimulation led to a reciprocal attenuation of MPFC activity (BA 10), but this pattern did not exist in cocaine users. No relationship was found between regional diffusion metrics and functional activity. Considered together these data suggest that, when engaged, cocaine users can mobilize their executive control system similar to controls, but that the 'set point' for mobilizing their limbic arousal system has been elevated-an interpretation consistent with opponent process theories of addiction.
Persistent oxidative stress depletes reduced glutathione (GSH), an intracellular antioxidant and an important determinant of CNS injury after hypoxia ischemia. We used standard, short echo time Stimulated Echo Acquisition Mode (STEAM) to detect GSH by magnetic resonance spectroscopy (MRS) in 24 term neonates with hypoxic-ischemic encephalopathy (HIE), on day of life 5-6, after rewarming from therapeutic hypothermia. MRS demonstrated reliable, consistent GSH of 1·64 ± 0·20 mM in the basal ganglia immediately before intravenous infusion of N-acetylcysteine. N-acetylcysteine resulted in a rapid and significant GSH increase to 1·93 ± 0.23 mM within 12-30 min after completion of infusion ( n = 21, p < 0.0001, paired t-test), compared with those who did not receive N-acetylcysteine ( n = 3, GSH = 1.66 ± 0.06 mM and 1.64 ± 0.09 mM). In one perinatal stroke patient, GSH in the diffusion-restricted stroke area was 1.0 mM, indicating significant compromise of intracellular redox potential, which also improved after N-acetylcysteine. For comparison, GSH in healthy term neonates has been reported at 2.5 ± 0.9 mM in the thalamus. This is the first report to show persistent oxidative stress reflected in GSH during the subacute phase in neonates with HIE and rapid response to N-acetylcysteine, using a short echo MRS sequence that is available on all clinical scanners without spectral editing.
The fiber orientation density function (fODF) in white matter is a primary physical quantity that can be estimated with diffusion MRI. It has often been employed for fiber tracking and microstructural modeling. Requirements for the construction of high fidelity fODFs, in the sense of having good angular resolution, adequate data to avoid sampling errors, and minimal noise artifacts, are described for fODFs calculated with fiber ball imaging. A criterion is formulated for the number of diffusion encoding directions needed to achieve a given angular resolution. The advantages of using large b-values (≥6000 s/mm 2 ) are also discussed. For the direct comparison of different fODFs, a method is developed for defining a local frame of reference tied to each voxel's individual axonal structure. The Matusita anisotropy axonal is proposed as a scalar fODF measure for quantifying angular variability. Experimental results, obtained at 3 T from human volunteers, are used as illustrations.
Purpose
To demonstrate how triple diffusion encoding (TDE) MRI can be applied to separately estimate the intra‐axonal and extra‐axonal diffusion tensors in white matter (WM).
Methods
Using a TDE pulse sequence with an axially symmetric b‐matrix, diffusion MRI data were acquired at 3T for 3 healthy adults with an axial b‐value of 4000 s/mm2, a radial b‐value of 307 s/mm2, and 64 diffusion encoding directions. This acquisition was then repeated with the radial b‐value set to 0. A previously proposed theory was applied to these data in order to estimate the intra‐axonal diffusivity and axonal water fraction for each WM voxel. Conventional single diffusion encoding data were also obtained with b‐values of 1000 and 2000 s/mm2, which provided additional information sufficient for determining both the intra‐axonal and extra‐axonal diffusion tensors.
Results
From the TDE data, the average intra‐axonal diffusivity in WM was found to be 2.24 ± 0.18 µm2/ms, and the average axonal water fraction was found to be 0.60 ± 0.11. From the 2 diffusion tensors, average WM values were estimated for several compartment‐specific diffusion parameters. In particular, the extra‐axonal mean diffusivity was 1.09 ± 0.19 µm2/ms, the intra‐axonal fractional anisotropy was 0.50 ± 0.14, and the extra‐axonal fractional anisotropy was 0.23 ± 0.13.
Conclusion
By using a simple TDE pulse sequence with an axially symmetric b‐matrix, the diffusion tensors for the intra‐axonal and extra‐axonal spaces can be separately estimated in adult WM. This allows one to determine compartment‐specific diffusion properties for these 2 water pools.
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